Microglia and astrocyte activation in the frontal cortex of rats with experimental autoimmune encephalomyelitis

- There is neuroinflammation in the brain cortex during the first hours of acute EAE onset.
- Neuroinflammation comprises activation of microglia and astrocytes, with no evident leukocyte infiltration.
- Alterations correlate with increased expression of pro-inflammatory cytokines.
- Neuroinflammation is restricted to the frontal region of the cortex.
- This work broadens previous findings of presynaptic alterations in the frontal cortex during EAE.

Experimental autoimmune encephalomyelitis (EAE) is a widely used animal model for the human disease multiple sclerosis (MS), a demyelinating and neurodegenerative pathology of the central nervous system. Both diseases share physiopathological and clinical characteristics, mainly associated with a neuroinflammatory process that leads to a set of motor, sensory, and cognitive symptoms. In MS, gray matter atrophy is related to the emergence of cognitive deficits and contributes to clinical progression. In particular, injury and dysfunction in certain areas of the frontal cortex (FrCx) have been related to the development of cognitive impairments with high incidence, like central fatigue and executive dysfunction. In the present work we show the presence of region-specific microglia and astrocyte activation in the FrCx, during the first hours of acute EAE onset. It is accompanied by the production of the pro-inflammatory cytokines IL-6 and TNF-α, in the absence of detectable leukocyte infiltration. These findings expand previous studies showing presynaptic neural dysfunction occurring at the FrCx and might contribute to the understanding of the mechanisms involved in the genesis and prevalence of common MS symptoms.